UBE2C promotes pancreatic tumorigenesis by KRAS stabilization via APC/C-mediated WDR76 degradation.

Bioinformatics-based association study revealed a strong positive correlation between UBE2C, an E2 ubiquitin-conjugating enzyme, and pancreatic cancer and patient survival. However, whether and how UBE2C plays a causal role in pancreatic tumorigenesis remains elusive. Here, we report that UBE2C functions as a promoter in this process.

DEPTOR suppresses lymphomagenesis by promoting EGFR degradation via HUWE1 E3 ligase.

DEPTOR, a naturally occurring inhibitor of mTOR, plays crucial roles in tumorigenesis and is frequently dysregulated in a variety of human cancers. Interestingly, DEPTOR could act either as a tumor suppressor or as an oncogene in a manner dependent of cellular context or tissue environment. Whether and how DEPTOR regulates lymphomagenesis remains elusive.

The FBXW7-RPAP2 Axis Controls the Growth of Hepatocellular Carcinoma Cells and Determines the Fate of Liver Cell Differentiation.

RNA polymerase II-associated protein 2 (RPAP2) plays a critical role in transcriptional regulation. However, little is known about whether and how RPAP2 regulates hepatocellular carcinoma (HCC) cell growth, and how the RPAP2 stability is precisely maintained. Here it is reported that high RPAP2 levels in HCC tissues correlate with poor patient survival.

The Cross Talk Between p53 and mTOR Pathways in Response to Physiological and Genotoxic Stresses.

The tumor suppressor p53 is activated upon multiple cellular stresses, including DNA damage, oncogene activation, ribosomal stress, and hypoxia, to induce cell cycle arrest, apoptosis, and senescence. Mammalian target of rapamycin (mTOR), an evolutionarily conserved serine/threonine protein kinase, serves as a central regulator of cell growth, proliferation, and survival by coordinating nutrients, energy, growth factors, and oxygen levels. p53 dysfunction and mTOR pathway hyperactivation are hallmarks of human cancer.